Atelectasis and ARDS Flashcards
What is the definition of atelectasis
state at which the lung in whole or in part is **collapsed **or without air: loss of lung volume d/t inadequate expansion of airspaces
What are the four types of atelectasis?
Resorption
compression
loss of surfactant
contraction
In Resorption atelectasis, what is the consequence of complete airway obstruction?
stops air reaching alveoli
get resoprtion of air trapped in distal airspaces via pores of Kohn
lack of air in distal airspaces adn collapse
In resoprtion atelectasis, where does obstruction occur?
bronchi, subsegmental bronchi or bronchioles
What are some causes of obstruction in resorption atelectasis?
Mucus plug, following surgery
aspiration of foreign material
bronchial asthma/bronchitis/bronchiectasis
Bronchial neoplasmas
What is the commenest cause of fever 24-36 hrs following surgery?
resoprtion atelectatis; see fever and dyspnea
In Resorption atelectasis we see _____deviation of trachea and _____diaphragmatic elevation
ipsilateral
ispilateral
Breath sounds and tactile fremitus increase/decrease/are absent in resorption atelectasis
both are absent
*collapsed lung doesn’t expand on inspiration
Aor or fluid accumulation in pleural cavity–increased pressure–collapses underlying lung
Compression atelectasis
tension pneumothorax and pelural effusion are both examples of
compression atelectasis
in compression atelectass, the trachea and mediastinum shift ____ from the atelectatic lung
AWAY
What do we notice about the lung in a patient with compression atelectasis?
lung field is hypertranslucent dt accumulation of air and collapse goesa way from collapsed lung
What do we see on this HE of alveoli
collapsed alveoli with minimal white space
In neonatal atelectasis, what causes collapse of alveoli?
loss of surfactant; especially issues with phosphatidlyglycerol
Surfactant proteins A and D are responsible for _____
Surfactant proteins B and C are responsible for _____
innate immunity
reduction of surface tension at air liquid barrier in alveoli
Surfactant is produced by _______ and begins at the ______ of gestation and stored in _______
produced by type 2 pneumocytes
synthesis begins by 28th week
stored in lamellar bodies
Synthesis is modulated by different hormones
____ and ____ Increase production
_____decreases production
cortisol and thyroxine increase
insulin decreaes
RDS in newborns is from decreased surfactant in fetal lungs, it can be a result of:
prematurity
maternal diabetes = increaesd insulin = decreased surfactant production
Cesarean section; labor + vaginal delivery increases stress related cortisol secreation adn increases surfactant production
Collapsed alveoli are lined with
hyaline membrane
In neonatal atelectasis, we see respiratory distress within in a few hours, see ________ and _______
What do we see on xray?
hypoxemia and respiratory acidosis
ground glass apperance
What complications arrive from neonatal atelectasis?
intraventricular hemorrhage
patent ductuas arteriosus (persistant hypoxemia)
hyoglycemia (excessive insulin release)
O2 therapy-damage to lungs and cataracts
in a premature infant, we see decreaed alveolar surfactant which leads to increaed alveolar tension and atelectasis which leads to:
uneven perfusion and hypoventilation
leads to acidosis
See fibrotic atelectasis in lung or pleura prevents full expansion, this is not reversible. What kind of atelectasis is this?
contraction atelectasis
Acute lung injury can be to what areas of lung>
endothelial and epithelial
Acute lung injury can be heritable and non heritable and is mediated by:
cytokines, oxidants, growth factors; TNF, IL-1, 6 and 10 adn TGF-Beta
What are the different manifestations we see from acute lung injury?
pulmnary edema, diffuse alveolar damage (ARDS)
Pulmonary edema is edema due to:
alterations in Starling pressure
we have increased hydrostatic pressure in pulmonary capillaries
Decreased oncotic pressure
Transudate
Edema fluid accumulation in alveoli w/ heart fail cells adn brown induration
In acute lung injury we see incrased hydrostatic pressure in pulmonary capillaries which causes:
left sided heart failure, volume overload, mitral stenosis and hemodynamic disturbances–cardiogenic pulmonary edema
In acute lung indury decreased oncotic pressure leads to
nephrogenic syndrome, liver cirrhosis
In acute lung injury, we see micovascular or alveolar injury to increase capillary permeability… what are those causes?
infection, aspiration, drugs, shock or traum and high altitude
whats going on in these cells?
Hemosiderin laden macrophages = heart fail cells from acute lung injury and edema
ARDS is alveolar injury, we get noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage; results in:
direct lung injury and indirect lung injury
What are the big risks for noncardiogenic pulmonary edema, results from
Gram negative sepsis (40%)
Aspiration (30%)
Severe trauma (10%)
pulmonary infections
Sepsis, diffuse lung infection, gastric aspiration adn physical injury are conditions assoicated with
ARDS
What clincal findings do se wee in ARDS?
dysnpea, severe hypoxemia, NOT responsive to O2 therapy and respiratory acidosis
In ARDS we see acute injury to epi or endo cell and alveolar macrophages release cytokines, this results in
neutrophil chemotaxsis, transmigration of neutrophils from caps into alveoli, leakage of protein(fibrin) exudate forming hyaline membrane and damage to pneumocytes–> causing low surfactant and atelectasis
Prognosis of ARDS is poor with ____ mortality. This is due to
60% mortality
progresive interstital fibrosis
What do we see on a cellular level in ARDS
sloughed bronchial epithelium
necrotic type I cell
edema fluid
cellular debris
hyaline membrane formation
neutrophil migration
Days post injury: we see edema peak at day ___ in the ____ phase
1
exudative phase
Hyaline membrane production peaks during day _____ and declines a few days later in the ____ phase
day 3, exudative phase
Interstitial inflammation and interstitial fibrosis peak during what day and what phase?
day 10
proliferative phase
